Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cyclosporin A (CsA) induces neurological side effects in up to 40% of patients. A reversible posterior leukoencephalopathy syndrome is the most serious complication. Symptoms include headache, altered mental functioning, seizures, cortical blindness, and other visual disturbances, with hypertension. Neuroimaging studies show white matter changes in the posterior regions of the brain. Other neurological side effects of CsA include tremor, diffuse encephalopathy, cerebellar syndrome, extrapyramidal syndrome, pyramidal weakness, and peripheral neuropathy. Hypertension, hypomagnesemia, hypocholesteremia, and the vasoactive agent endothelin may all play a role in the pathogenesis of CsA neurotoxicty. Neurotoxicity is more frequent with high CsA blood levels, but levels may be within the therapeutic range. Dose reduction or withdrawal of CsA usually results in resolution of clinical symptoms and of neuroimaging abnormalities.
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PMID:Cyclosporine neurotoxicity: a review. 1039 63

Two women (aged 12 and 32 years) and a man aged 40 years presented with fluctuating confusional states, depressed level of consciousness, seizures and tremor or myoclonic activity; hallucinations occurred in two of them. Laboratory examinations showed antibodies to thyroid peroxidase in serum, elevated protein levels in CSF and normal cerebral MRI. The EEG findings were indicative of diffuse encephalopathy. Hashimoto's encephalopathy was diagnosed. One patient improved dramatically on prednisone therapy, the other two patients recovered spontaneously. Hashimoto's encephalopathy is a subacute, fluctuating encephalopathy with combinations of impaired level of consciousness, involuntary movements, and epileptic or psychiatric symptoms. It occurs in patients with antithyroid antibodies. It is important to consider this diagnosis, since some patients may benefit from treatment with corticosteroids.
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PMID:[Variable manifestations of Hashimoto's encephalopathy]. 1041 87

The most venomous scorpion species are Buthotus tamulus of India, the Leiurus quinquestriatus and Androctonus crassicauda of North Africa and the Middle East, the Tityus serrulatus of Brazil, and the Centruroides suffussus of Mexico. The severity of scorpion envenomation varies with the scorpion's species, age, and size, and is much greater in children. Systemic intoxication reflects the overstimulation of the CNS, the sympathetic and parasympathetic nervous system. Severity ranges from local pain and paresthesia to fatal cardiotoxicity and encephalopathy. Symptoms include: agitation, tachycardia, vomiting, abdominal pain, salivation, diaphoresis, dehydration, muscle rigidity and twitching, tremor, seizures, coma, pupillary changes, hyperthermia, tachyarrythmias and occasionally bradyarrhythmias, hypertension, and less often hypotension, cardiac failure, and priapism in males. Laboratory abnormalities include: hyperglycemia, leucocytosis, transient elevation of cardiac and pancreatic enzymes, ischemic changes in the ECG, and evidence of cardiac dysfunction on echocardiography. The principles of management are: observation, cardiac monitoring, supportive treatment with intravenous fluids and electrolytes, and a meticulous use of cardiovascular agents: vasodilators, adrenergic antagonists, or calcium channel blockers in the hypertensive phase; and inotropic agents in the event of hypotension. Antiarrhythmics such as lidocaine, may be required. There is increasing evidence for the efficacy of specific antivenom. The advance in supportive care and antivenom efficacy has markedly improved the outcome of patients with scorpion envenomation.
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PMID:Clinical manifestations and management of scorpion envenomation. 1044 63

A case of acute encephalopathy with selective bilateral symmetrical striatal lesions is reported. The patient was a previously healthy 4-year-old boy who became obtunded after a febrile illness and fell into a state of delirium with severe pain in the feet. He showed abnormal postures: hyperextension of the neck and upper limbs and extreme flexion of both lower limbs, and abnormal involuntary movements of the limbs: tremor, athetotic movement and right hemiballismus. Analysis of serum antibody titres suggested recent primary infection of herpes simplex type 1 (HSV-1). Cranial T2-weighted magnetic resonance imaging (MRI) demonstrated areas of high-signal intensity involving the whole basal ganglia bilaterally. He showed rapid clinical improvement after the initiation of corticosteroid therapy; complete clinical recovery was noted 3 months after the onset. Serial MRI studies demonstrated a rapid reduction of the lesions, resulting in only slight T2-hyperintense areas in both caudate nuclei. The pathogenesis of the disorder remains unknown, though an autoimmune mechanism has been speculated. The clinical and laboratory findings in this case suggested a possible role of HSV-1 in the pathomechanism of the disorder and a beneficial effect of early corticosteroid therapy.
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PMID:Acute encephalopathy with bilateral striatal necrosis: favourable response to corticosteroid therapy. 1072 92

Hashimoto's encephalopathy is a poor understood neurological disorder associated with thyroid disease. We describe a 12 years old woman with a relapsing clinical picture characterized by acute onset confusion, tremor, convulsive seizures and a stroke-like episode associated with autoimmune thyroid disease. High titers of antithyroid antibodies were detected in her serum. Neurologic investigation showed a marked slowing of the basic activity in EEG, diminished perfusion of left hemisphere in brain SPECT, mild CSF protein level without pleocytosis, and normal brain CT and cerebral angiogram. The clinical course was favorable without corticosteroid therapy. Antithyroid antibodies and EEG were normal after one-year follow-up. We suggest that antithyroid antibody levels should be checked in any unexplained acute or subacute encephalopathy, especially when a relapsing course, stroke-like exacerbation, seizures, tremor or elevation of the CSF protein are found.
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PMID:[Hashimoto's encephalitis: a new case with spontaneous remission]. 1107 81

We report the clinical laboratory, electroencephalography (EEG), magnetic resonance imaging (MRI) and single photon emission computerized tomography (SPECT) findings in a 15 year-old euthyroid girl with autoimmune thyroiditis and encephalopathy. She had stupor, coma and generalized tonic clonic seizure preceded by tremor and myoclonus with a previous misdiagnosis of epilepsy and encephalitis. Response to steroid after the 3rd relapse was excellent. Another four children in the literature are also discussed.
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PMID:Tremor and myoclonus heralding Hashimoto's encephalopathy. 1108 93

Neurologic manifestations are rarely described in hereditary hemochromatosis (HH). We describe three patients with HH and movement disorders. Patient 1, a 69-year-old man, had a 13-year history of disabling cerebellar syndrome, action tremor and myoclonus, and secondary dementia. Patient 2 was a 40-year-old man with a 9-year history of cerebellar syndrome, head and arm tremor, and cervical dystonia. Patient 3, a 75-year-old woman, had a 5-year history of rapidly disabling parkinsonian syndrome unresponsive to levodopa. The diagnosis of HH was established in the three patients by iron tests, evidence of a C282Y mutation, and, in two patients, by liver biopsy. High-field T2-weighted magnetic resonance imaging showed hyperintense signals in hemispheric white matter in patient 1, cerebellar atrophy in patient 2, and cerebellar and cerebral atrophy in patient 3 and no significant hypointense signals in the three patients. Phlebotomies and symptomatic treatments did not change the course of the disease. Our cases are compared with the five previously reported observations of HH with movement disorders. This rare association is one cause of the chronic acquired non-Wilsonian hepatocerebral degeneration syndromes and represents a separate entity from aceruloplasminemia. The pathophysiologic mechanism of movement disorders in HH is unresolved. No hepatic insufficiency and portosystemic encephalopathy is evidenced in our cases, whereas the putative role of abnormal iron load remains to be ascertained. HH should be investigated more systematically in patients with movement disorders.
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PMID:Clinical report of three patients with hereditary hemochromatosis and movement disorders. 1110 6

This paper gives an overview of the clinical importance of SPECT and PET imaging of the dopaminergic system in the differential diagnosis and for the determination of the progression rate of Parkinson's disease (PD). D2 receptor imaging can help to differentiate multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) from PD. In patients treated with neuroleptics it is possible to determine the rate of striatal D2 receptor blockade using this technique. This occupancy rate parallels the occurrence of parkinsonian side effects. Its measurement helps in the selection of newer atypical neuroleptics, which can be used to treat drug-induced psychosis in PD because they do not aggravate parkinsonian symptoms. Imaging of dopaminergic neurons with [123I]beta-CIT SPECT or [18F]DOPA PET is a way to visualize and quantify the nigrostriatal dopaminergic lesion in PD. Findings correlate with clinical rating scales and demonstrate the feasibility of detecting the preclinical lesion in patients with hemiparkinson or familial PD. [123I]beta-CIT SPECT can easily distinguish patients with essential tremor and patients with "lower body parkinsonism" due to a subcortical vascular encephalopathy. MSA and PSP cannot be separated from PD with this method alone. Longitudinal studies with [123I]beta-CIT SPECT and [18F]DOPA PET can quantify the progression rate in PD. SPECT results from our own group show a low rate of progression in patients with a long duration of disease and a more marked progression rate in patients with shorter disease duration. In the former group regions in the striatum with higher beta-CIT binding at the time of the first SPECT scan decline faster than regions with lower binding. These findings suggest a curvilinear course of progression which starts at different time points in different striatal regions and which levels off after several years of disease duration. These findings are in line with data from PET studies and underline the importance of an early start of neuroprotective strategies. Preliminary data from PET and SPECT studies in early PD suggest that dopamine agonists might have a slight neuroprotective effect and might slow down the rate of progression of the disease.
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PMID:SPECT and PET imaging of the dopaminergic system in Parkinson's disease. 1119 11

Portal-systemic encephalopathy may be seen with hyperammonemia that complicates chronic liver disease. We report an unusual case of reversible parkinsonism associated with hyperammonemia and portal vein thrombosis. An active 90-year-old male developed motor slowing and resting hand tremor over 6 months. Examination showed asterixis, bradykinesia, cogwheel rigidity, rest tremor, and a parkinsonian gait. Serum venous ammonia was elevated at 145 microM. The next day, the patient became comatose and serum ammonia was 178 microM. With lactulose therapy, serum ammonia level normalized and examination showed only minimal parkinsonism after 1 week. An abdominal CT scan identified portal vein thrombosis with porto-systemic shunting that reversed after 7 months of treatment. Examination 2 years later showed no signs of parkinsonism. Parkinsonism can dominate the clinical picture of patients with hyperammonemia before the onset of encephalopathy.
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PMID:Reversible parkinsonism and hyperammonemia associated with portal vein thrombosis. 1124 May 69

Myoclonus, defined as shock-like involuntary movement, may be physiological or caused by a very wide variety of hereditary and acquired conditions. Because myoclonus can originate from different disorders and lesions affecting quite varied levels of the central and peripheral nervous systems, it represents from many points of view a diagnostic challenge. Moreover, new entities have been recently individualized, such as cortical tremor, which deserve renewed attention. The aim of this review is to propose a rationale for a diagnostic approach based on clinical and electrophysiological grounds. In this setting, we successively address 1) the clinical features allowing a positive diagnosis of myoclonus; 2) the clinical clues to the etiology; 3) the relevance of the clinical context to the diagnosis; and 4) the contribution of neurophysiology. Differentiating myoclonus from tics, spasm, chorea and dystonia can be difficult, and a careful reappraisal of clinical features allowing precise identification is presented. Moreover, the topographical distribution of myoclonus, the temporal pattern of muscle recruitment, the condition of occurrence and the rhythm of the event, may provide clinical clues relevant to the diagnosis. Myoclonus without associated epilepsy, myoclonus with epilepsy, myoclonus with encephalopathy, parkinsonism and/or dementia represent overlapping clinical categories, although they remain useful for the diagnostic approach. Using electrophysiology (including back-averaging EEG, MEG, SEP, C-reflex studies) to determine the origin of myoclonus may not allow us to focus on the underlying condition. Indeed, in many instances, the myoclonus is cortical in origin, but the pathology is found elsewhere.
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PMID:[Myoclonus in the adult: diagnostic approach]. 1128 Oct 67


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